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目的:研究杨梅素(myricetin,YMS)抗离体心脏心肌缺血再灌注损伤作用。方法:将实验分为正常组、模型组、YMS组与YMS+GW9662(PPARγ的选择性阻断剂)组。采用Langendorff造模方法,利用生物多导记录仪连续测定血流动力学参数,TTC染色法检测心脏梗死面积。ELISA法检测白介素6(IL-6)、C反应蛋白(CRP)和肿瘤坏死因子α(TNF-α)的含量。通过Western blot方法检测心肌组织中过氧化物酶增殖物激活受体γ(PPARγ)和NF-κB的蛋白表达。结果:与正常组相比较,模型组出现严重的心脏功能障碍和较大的心肌梗死面积,心肌组织中CRP,IL-6和TNF-α含量增加,心肌组织中NF-κB的蛋白表达量显著升高。与模型组对比,YMS组的心脏功能显著恢复,心肌梗死面积明显降低;心肌组织中CRP,IL-6和TNF-α含量显著降低,YMS组PPARγ的表达量显著升高,而NF-κB的表达量显著降低。YMS的这种心脏保护作用几乎全部被GW9662阻断。结论:YMS具有显著的抗心肌缺血再灌注损伤作用,其机制可能与PPARγ/NF-κB信号通路有关。
Objective: To study the effect of myricetin (YMS) on myocardial ischemia reperfusion injury in vitro. Methods: The experiment was divided into normal group, model group, YMS group and YMS + GW9662 (PPARγ selective blocker) group. The Langendorff modeling method was used to measure the hemodynamic parameters continuously with a bio-polyspectrum recorder. The infarct size was detected by TTC staining. The levels of interleukin 6 (IL-6), C-reactive protein (CRP) and tumor necrosis factor alpha (TNF-alpha) were detected by ELISA. The protein expression of peroxisome proliferator-activated receptor γ (PPARγ) and NF-κB in myocardium was detected by Western blot. Results: Compared with the normal group, the model group showed severe cardiac dysfunction and larger myocardial infarction area. The contents of CRP, IL-6 and TNF-α in myocardial tissue increased and the expression of NF-κB protein in myocardial tissue was significant Rise. Compared with the model group, the cardiac function of YMS group was significantly recovered, and the area of myocardial infarction was significantly reduced. The content of CRP, IL-6 and TNF-α in myocardium was significantly decreased, while the expression of PPARγ in YMS group was significantly increased The amount of expression is significantly reduced. This cardioprotection of YMS is almost completely blocked by GW9662. Conclusion: YMS has significant anti-myocardial ischemia-reperfusion injury and its mechanism may be related to PPARγ / NF-κB signaling pathway.